Apoptosis in Cardiac Biology
Heribert Schunkert, G.A.J. Riegger
Springer Science & Business Media, Nov 30, 1999 - Medical - 354 pages
Apoptosis or programmed cell death is increasingly considered to be a major factor in the development and progression of cardiovascular disease. In patients with heart failure the activation of apoptosis may result in the loss of irreplaceable cardiac myocytes promoting the clinical course of the syndrome. Moreover, in the coronary arteries inflammation and apoptosis may weaken critical structures of the vessel wall leading to plaque rupture and, subsequently, to myocardial infarction. Given these deleterious consequences, it seems almost paradoxical that programmed cell death is an active process that, if initiated under physiological circumstances, is essential for both coordinated tissue growth or destruction of malignant cells.
Apoptosis in Cardiac Biology, written by a team of internationally renowned researchers, gives a timely synopsis of basic mechanisms, cellular and structural targets and, finally, clinical implications of programmed cell death in the heart. The expert authors of this volume give concise overviews on general and cell-specific aspects of programmed cell death in cardiac myocytes and fibroblasts, as well as in vascular smooth muscle and endothelial cells. Furthermore, novel therapeutic options arising from the outstanding pathophysiological significance of cardiac apoptosis are presented.
This comprehensive review of Apoptosis in Cardiac Biology will be of interest to both clinicians and basic researchers who are active in the fields of cardiology and atherosclerosis.
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angiotensin Anversa apoptosis in cardiac apoptosis induced Bcl-2 family binding Biochem Biol Chem cardiac ﬁbroblasts cardiac myocytes Cardiol cardiomyocyte apoptosis cardiomyocytes cardiovascular carvedilol cascade caspase caspase-3 caspase-9 cell cycle cellular Circ Res Circulation cleavage Clin Invest collagen congestive heart failure coronary cultured cyclin cytochrome cytokines cytoplasmic cytosolic death domain death receptors disease DNA fragmentation effect endothelial cells estrogen fibroblasts ﬁndings function gene expression growth factor human hypertensive hypertrophy hypoxia identiﬁed increased induces apoptosis induction of apoptosis inhibition inhibitor interaction interleukin intracellular ischemia ischemic Kajstura lesions ligand lymphocytes macrophages mechanisms mediated mice mitochondrial membrane molecular molecules mRNA myocardial infarction myocardium myocyte apoptosis neonatal nitric oxide Oncogene overexpression patients phosphorylation programmed cell death protein kinase Reed JC regulation release reperfusion response role senescent signaling pathways signiﬁcant signiﬁcantly smooth muscle cells speciﬁc stimulation studies tissue tumor necrosis factor TUNEL undergo apoptosis vascular vitro vivo VSMCs Wang